In this study, we demonstrate that variant genotypes in TLR-2, TLR-4 and TLR-9 genes are associated with an increased bacterial antigen burden and a decreased pro-inflammatory cytokine profile in blood of patients with cirrhosis and non-infected AF, suggesting that these genetic variants may compromise bacterial antigen interaction with their specific receptors and limit the innate soluble inflammatory response in these patients. The gene discussed is TLR9; the disease is atrial fibrillation.